Defect of a complement receptor 3 epitope in a patient with systemic lupus erythematosus.

T Witte; F L Dumoulin; J E Gessner; J Schubert; O Götze; C Neumann; R F Todd; H Deicher; R E Schmidt

doi:10.1172/JCI116688

Published September 1, 1993 - More info

View PDF

Abstract

Complement receptor 3 (CR3) is expressed on cells of the reticuloendothelial system and involved in the clearance of immune complexes. In this article a patient with a deficiency of the C3bi binding site of this receptor is described. Clinically this patient exhibited predominantly cutaneous manifestations of a systemic lupus erythematosus with an immune vasculitis and panniculitis. The deficiency of the CR3 epitope was demonstrated using flow cytometry. The functional relevance of this defect was demonstrated in a rosetting assay with C3bi-loaded erythrocytes. C3bi binding was found to be significantly decreased. Furthermore, there was an impairment of phagocytosis of opsonized Escherichia coli. The CR3 defect is not due to an autoantibody but is assumed to have a genetic basis. These data suggest that the defect of the CR3 may be involved in the pathogenesis of the immune vasculitis in this patient.

Images.

Defect of a complement receptor 3 epitope in a patient with systemic lupus erythematosus.

T Witte, F L Dumoulin, J E Gessner, J Schubert, O Götze, C Neumann, R F Todd 3rd, H Deicher, and R E Schmidt

Article tools

Metrics

Go to

Defect of a complement receptor 3 epitope in a patient with systemic lupus erythematosus.

T Witte, F L Dumoulin, J E Gessner, J Schubert, O Götze, C Neumann, R F Todd 3rd, H Deicher, and R E Schmidt

Article tools

Metrics

Go to

Sign up for email alerts